Antiviral drugs for herpesviruses, CMV and influenza
How aciclovir, valaciclovir, ganciclovir, foscarnet, cidofovir, letermovir, maribavir and the influenza antivirals work, why activation by viral kinases explains their selectivity and resistance, and the mechanisms of their kidney, marrow and electrolyte toxicity.
Tier 2Medical sciences concept
Written with AI assistance and fact-checked against the sources below. For exam study, not clinical decisions. How notes are made
At a glance
- Most antivirals for herpesviruses are nucleoside analogues that need phosphorylation. The first step is done by a viral kinase (HSV/VZV thymidine kinase, CMV UL97), which gives selectivity and is the usual site of resistance.
- Drugs that skip viral activation (foscarnet, cidofovir) still work against kinase-mutant virus but are more toxic to the kidney.
- Newer CMV drugs work outside the polymerase: letermovir (terminase) for prophylaxis, maribavir (UL97 inhibitor) for refractory or resistant disease, PBS listed (S100 Highly Specialised Drugs, public hospital, Authority required (Streamlined)).
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Sources
- Therapeutic Guidelines: AntibioticAU/NZTherapeutic Guidelines Limited
- Australian Medicines HandbookAU/NZAustralian Medicines Handbook Pty Ltd, 2026
- Maribavir (Livtencity): PBS medicine status and public summary document, November 2024 PBAC meetingAU/NZPharmaceutical Benefits Scheme, 2025
- Letermovir prophylaxis for cytomegalovirus in hematopoietic-cell transplantationNew England Journal of Medicine (Marty et al.), 2017
- Goodman & Gilman's The Pharmacological Basis of Therapeutics (14th ed.)McGraw Hill (Brunton and Knollmann, 2023), 2023
- Last updated
- 14 November 2026
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